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KG - Pharmacology > Sulfonamides & Miscellaneous Antibiotics > Flashcards

Sulfonamides & Miscellaneous Antibiotics Flashcards

1
Q

pharmacodynamics of sulfonamides

A
  • only antibiotics that target metabolic pathway
  • target folic acid pathway
  • compete w/ para-aminobenzoic acid (PABA) for incorporation into folic acid
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2
Q

characteristics of sulfonamides

A
  • all sulfa drugs derivatives of benzene sulfanilamide (sulfonamide) having similar antibacterial action
  • produced by substitution at amino group
  • differences based on rate of absorption, excretion, solubility in urine, etc…
  • for antibacterial action, free para amino group essential
  • bacteriostatic
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3
Q

list of sulfonamides

A
  • SULFAMETHOXAZOLE + TRIMETHOPRIM, CO-TRIMOXAZOLE, TMP-SMX (BACTRIM) - oral/parenteral –> all same thing but different names
  • sulfamethoxazole (gantanol) – slow excretion, high urine concentration – ORAL
  • sulfasalazine (azulfidine) – GI action, ulcerative colitis – ORAL
  • silver sulfadiazine (silvadene) – burns – topical
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4
Q

mechanisms of SULFAMETHOXAZOLE + TRIMETHOPRIM, CO-TRIMOXAZOLE, TMP-SMX (BACTRIM)?

A
  • sulfamethoxazole competes w/ PABA in synthesis of bacterial FOLIC ACID
  • trimethoprim prevents reduction of dihydrofolate to tetrahydrofolate (which is essential for one carbon transfer)
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5
Q

what does sulfadoxine + pyrimethamine do to help w/ malaria?

A
  • inhibits DHFR (dihydrofolate reductase)
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6
Q

what is sulfadiazine + pyrimethamine for?

A

toxoplasmosis

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7
Q

what is methotrexate for?

A

anti-cancer drug, inhibits rapidly growing cells/DHFR

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8
Q

resistance of SULFAMETHOXAZOLE + TRIMETHOPRIM, CO-TRIMOXAZOLE, TMP-SMX (BACTRIM)

A
  • increased production of essential metabolite or drug antagonist (PABA)
  • active efflux or decreased permeability
  • alternative metabolic pathway for synthesis of essential metabolite (plasmid)
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9
Q

characteristics of SULFAMETHOXAZOLE + TRIMETHOPRIM, CO-TRIMOXAZOLE, TMP-SMX (BACTRIM)

A
  • generally bacteriostatic
  • in urinary tract bactericidal concentration may be attained
  • sulfa drugs inhibit both G- and G+ organisms
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10
Q

therapeutic uses of sulfonamides?

A
  • UTIs (FIRST ATTACK), Co-trimoxazole = DOC
  • pneumocystitis jiroveci (carinii) infections in children & AIDS patients (prophylaxis)
  • chlamydia trachomitis - trachoma (azythro or tetracyclines are DOC)
  • toxoplasma gondii - sulfadiazine + pyrimethamine
  • sulfasalazine is a prodrug used in treatment of ulcerative colitis, active in arthritis
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11
Q

metabolism/absorption of SULFAMETHOXAZOLE + TRIMETHOPRIM, CO-TRIMOXAZOLE, TMP-SMX (BACTRIM)

A
  • oral admin, absorption adequately rapid
  • freely cross placenta & blood brain barrier, excreted in breast milk
  • urine concentration 10-20x plasma
  • sulfa drugs metabolized in liver as acetylated products and excreted through kidneys
  • CO-TRIMOXAZOLE available for IV use - only for extreme circumstances
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12
Q

contraindications of SULFAMETHOXAZOLE + TRIMETHOPRIM, CO-TRIMOXAZOLE, TMP-SMX (BACTRIM)

A
  • near term
  • nursing premature infants
  • jaundiced infants
  • never give to infants < 2 months age
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13
Q

toxicities of sulfa drugs

A
  • DRUG SENSITIVITY - allergy 6% (cross rxns w/ diuretics/celecoxib/some oral anti diabetic agents)
  • blood dyscrasia - aplastic anemia (G6PD)
  • kidney/liver damage, microscopic hematuria
  • peripheral nerve damage
  • Stevens-Johnson syndrome
  • photosensitivity
  • kernicterus
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14
Q

what class of antibiotics is Daptomycin (cubicin)?

A

lipopeptide antibiotics

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15
Q

mechanism of Daptomycin (cubicin)?

A
  • cyclic lipoprotein
  • don’t penetrate bacterial cytoplasm
  • binds to bacterial membranes and cause rapid depolarization of membrane potential
  • loss of membrane potential leads to inhibition of protein, DNA, RNA synthesis, and bacterial cell death
  • forms transmembrane cell channels - leakage of intracellular ions and depolarization
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16
Q

characteristics of daptomycin

A
  • lipopeptides appear to be bactericidal against G+ bacteria (MRSA, MSSA) - concentration dependent
  • aerobic, anaerobic
  • resistance rare
  • IV admin
  • half life 8-9 hrs - once daily dosing
  • 78% excreted by kidneys
17
Q

adverse rxns to daptomycin?

A
  • most rxns mild or moderate
  • candidiasis, general discomfort, fatigue, fever, flushing, hypersensitivity rxns, injection site rxns, rigors, weakness
  • suitable for empiric therapy in pts w/ serious G+ infections - alternate to vancomycin
18
Q

mechanism of MUPIROCIN (bactroban)

A
  • produced from pseudomonas fluorescens
  • structurally unrelated to other antibiotics
  • bacterial PROTEIN and RNA SYNTHESIS ARE INHIBITED when mupirocin reversibly binds to bacteria isoleucyl-tRNA synthetase
19
Q

characteristics of mupirocin (bactroban)?

A
  • good against G+ and some G-
  • BACTERIOSTATIC at low concentrations
  • BACTERICIDAL at high concentrations
  • admin topically to skin or nares
20
Q

what is used to treat IMPETIGO?

A

mupirocin (bactroban)

- impetigo caused by s. aureus and b-hemolytic streptococci incl strep pyogenes

21
Q

when would an intranasal application of mupirocin (bactroban) be used?

A
  • ppl who carry methicillin resistant strains of s. aureus (MRSA)
22
Q

why does mupirocin (bactroban) have little resistance with other antibiotics?

A

b/c of its unique mechanism

23
Q

name 2 polypeptide antibiotics

A
  • polymyxin B (aerosporin)

- colistin (polymyxin E)

24
Q

what infections are polypeptide antibiotics used for?

A

G- infections

25
Q

mechanism of action polypeptide antibiotics

A
  • polymyxin B binds to G- bacterial cell membrane phospholipids (lipid A of endotoxin)
  • binding increases permeability of cell membrane which results in loss of metabolites needed for bacterial existence
  • polymyxin B is bactericidal against most G- bacilli w/ exception of proteus and neisseria species (no effect in G+, lack endotoxin)
26
Q

in which bacteria does one find lipid A?

A

G-

27
Q

characteristics polypeptide antibiotics

A
  • no GI absoprtion (no oral use)
  • distribution after parenteral use poor
  • bound very well to plasma proteins
  • excretion through kidney is slow
28
Q

toxicity of polypeptide antibiotics

A
  • NEPHROTOXICITY - use topically
  • paresthesia, ataxia, dizziness
  • visual/speech disturbances, leukopenia, granulocytopenia
29
Q

use of polypeptide antibiotics

A
  • topical in combo w/ neomycin (aminoglycoside) and bacitracin (G+)
  • topical application to wounds, burns, etc (pseudomonas infections) and the eye

KG - Pharmacology (8 decks)

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